Title
Regulation of protein kinase C isozymes during early postnatal hippocampal development
Date Issued
08 September 2009
Access level
open access
Resource Type
journal article
Author(s)
Purkayastha S.
Fernando S.S.
Diallo S.
Cohen L.
Ranasinghe B.
Banerjee P.
The College of Staten Island (CUNY)
Abstract
During neonatal hippocampal development, serotonin 1A receptor-mediated signaling initially employs PKCe{open} to boost neuronal proliferation and then uses PKCα to promote synaptogenesis. Such stage-specific involvement of a PKC isozyme could be determined by its relative expression level. In mouse hippocampi, we detected relatively low levels of α, β, γ, and δ isozymes at postnatal days 2-6 (P2-6), which was followed by a large increase in their expression. In contrast, the PKC isozymes e{open} and θ were relatively abundant at P6, following which they underwent a further increase by P15. Comparison with purified proteins confirmed that the PKCe{open} levels at P6 and P15 were respectively 1.75 and 7.36 ng per 60 μg of protein, whereas PKCα levels at P6 and P15 were respectively 160 pg and 1.186 ng per 60 μg of protein. Therefore, at P6, PKCe{open} was about 11-fold more abundant than PKCα. Consequently, signaling cascades could use the relatively abundant PKCe{open} (and possibly PKCθ) molecules for early events at P2-6 (e.g. neurogenesis), following which PKCα (and the β, γ, or δ isozymes) could guide maturation or apoptosis. Notably, at P6 but not P15, PKCe{open}, was localized to the nuclei of neuroblasts, probably directing mitosis. In contrast, at P15 but not P6, PKCα was highly expressed in the processes of the differentiated hippocampal neurons. In summary, PKC isozymes follow differential profiles of expression in neonatal hippocampus and the relative abundance of each may determine its mode and stage of involvement in hippocampal development. © 2009 Elsevier B.V. All rights reserved.
Start page
29
End page
41
Volume
1288
Language
English
OCDE Knowledge area
Ciencias socio biomédicas (planificación familiar, salud sexual, efectos políticos y sociales de la investigación biomédica)
Neurología clínica
Subjects
Scopus EID
2-s2.0-69049096947
PubMed ID
Source
Brain Research
ISSN of the container
00068993
Sponsor(s)
This project was supported by a grant from the NIH (MH071376). Graduate assistantships from the Louis Stokes Alliance for Minority Participation (for K.L. and S.D.) are gratefully acknowledged here. The authors also acknowledge valuable technical advice from Dr. Tomasz A. Sobocki (Sophie Davis School of Bio-Medical Education, CUNY). Appendix A
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